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Definition of Asthma
Syndrome
etiopathogenic types
-extrinsic (alergic)
-profesional
EPIDEMIOLOGY
Factors influencing prevalence
age
maximal prevalence beetween 1-17 years and 45-64 years
asthmatic children present in 50 % of cases a full remission of de symptoms at puberty
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Hypothetical Representation of the Natural History of Asthma
Asthma
-Heterogeneous condition
-Lack of well-defined markers for the different disease phenotypes grouped under this common label
-Most cases of persistent asthma start in early life (first 5 years of life)
Natural history
-Many children have asthma-like symptoms during viral infections in the preschool years
-Most are transient conditions that subside with age
-Only a minority will have persistent asthma
-Hard to distinguish who will develop asthma
-an increased risk of wheeze by the age of 6 (risk decreased with age and became not significant by the age
of 13)
There was no association between RSV lower respiratory tract illnesses and subsequent atopic status
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Phenotypes of wheezing in childhood
Predisposing factors
-Maternal smoking during pregnancy
-Lower levels of lung function in the first months of life
Development of asthma
-Inverse relationship between duration of symptoms and level of lung function in school-age children with
asthma1
-Sensitization to local aeroallergens is strongly associated with increased risk of asthma in adult life
Asthma between school years and mid adult life is associated with:
-Sensitization to local aeroallergens
-Elevated total circulating IgE
-Both1
Hypothesis -Sensitization to specific allergens (early life) is the cause of asthma (IgE specific)
-Children with skin-test negative to Alternaria develop asthma-like symptoms in the first year of life
-Children with skin-test positive to Alternaria have peak incidence of asthma-like symptoms at age 2-3
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In both groups –inception of symptoms before age 3
-Non-atopic asthma develop earlier than atopic asthma (different mechanisms)
-Studies performed in low exposure to house dust mites areas –prevalence of asthma is similar or higher than
in areas with high exposure1
-N. Sweden (low indoor exposure to dust mites/molds ) –similar prevalence of school-age asthma with S.
Sweden (high exposure)2
-Most children with severe symptoms will develop severe symptoms in adulthood
-Most children with mild symptoms will develop mild/no symptoms in adulthood
-Allergic symptoms (rhinitis, eczema) are associated with persistence of asthma into adult life
-Factors associated with relapses of asthma in adulthood with symptoms remitted during teenage period –
unknown (appears to be independent of allergies and smoking)1
MORTALITY
UK, 1982 aparent higher prevalence of deaths among asthmatics by comparison with 1970 (>2 folds)
-1998 for first time the mortalitaty in BA is comparable with the general population
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Social impact
-USA there are 15 millions asthmatics
-In Romania there are 1 million asthmatics!
-Major cost of drugs
-Major costof frequent hospitalizations
-Major social economic cost by losing working days
Macro: distended lungs , circumscribed atelectasia by mucous plugs that were obstructing subsegmentary
bronchi.
Micro: important thikening of the bronchial wall (edema, glandular hiperplasia, thikening of the basal
membrane, thikening of the smooth muscle cell layer, important cellulear inflammatory infiltration especially
with eosinophils and lymphocytes); extensive necrosisof the bronchial epithelium with mucosal uncovering.
bronchial biopsy:microscopic features met in postmortem studies were found even in mild and medium
severe forms of asthma and even during clinical remission
broncho-alveolar lavage (BAL): a method able to identify and characterize the cells and the mediators
involved in asthmatic inflammation
-All the cells involved in the chain of the immune reactions will be also active in bronchial asthma
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Cellular mechanisms in BA Mecanisme celulare in AB
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CONCLUSIONS
1.Chronic inflammation: eosynophils
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BRONCHIAL HIPERREACTIVITY
Definition: the ability of the bronchi to decrease their diameter to stimuli that are usually indifferent
Types of stimuli:
Relation INFLAMMATION-BHR-SYMPTOMS
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CONCLUSIONS
-Chronic inflammation induces hyperreactivity
-Viral infections can trigger asthmatic exacerbations (but asthma is not an infection!)
-adjuvant: respiratory infections, air polution, smoking (active and second hand)
-professional,
-NSAI related,
-intrinsic,
BUT PRAGMATICAL
-Systematic search for a causal factor in the patient’s enviroment
Allergens
Indoor:
-mytes (main cause for sensitisation)
-fungi
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Outdoor:
-pollens (trees, grass, and ??)
-fungi
ASTHMA DIAGNOSIS
-Asthmatic symptoms
-Atopy
-Family history
Asthmatic symptoms
1-Dyspneea
-Usually dominant, rarely absent
->/< paroxystical
-expiratory
2-Wheezing
-Usually associated with dyspneea
-relatively specific
3-Cough
-rarely dominant, usualy associated to dyspneea
-sometimes severe
4-Chest tightness
-Associated with dyspneea
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Variable:
-Associated with trigger factors
1-Asthmatic crisis
2-Asthmatic exacerbation
3-Continuous symptoms
4-Coughing asthma
Physical examination
-Respiratory rate: normal or mildly enhanced
Diffuse wheezes
Spirometry:
-FEV1 (Forced Expiratory Volume in the first second)
-Peak-flow-metry
depends by:
Enhanced by:
repeating the measurement
ideal for measuring pulmonary function In the GP office & At home by the patient
-Improvement of PEF by more than 15% at 15-20 (max. 30) minute after bronchodilation (a short acting 2
agonist)
-Variable PEF more than 20% morning/evening and taking a bronchodilator (or more than 10% without taking
a bronchodilator)
-Reduction of PEF with more than 15% at 5-10 minutes after an effort (running) of 6 minutes
PEF chart
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Spirometry
-FEV1, VC si FEV1/VC = most validated functional respiratory parameters
3. COPD
8. Anxiety (Tachipnea)
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Bronchial asthma therapy
1. Patients education
3. Antiasthmatic drugs
4. Therapeutic strategy
6. Life-threatening asthma
-Don’t panic!
3. ANTIASTHMATIC DRUGS
-Antiasthmatics
-Controller (control) -Reliever (symptoms)
Antiasthmatics-”controller”
1. Inhaled corticosteroids
2. Systemiccorticosteroids
3. Theofylline
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5. Leukotrienemodifiers
6. Anti-IgE
Antiasthmatics-”reliever”
1. Short acting Beta 2 agonists
2. Systemic corticosteroids
3. Short acting Anticholinergics
Significance of the“controller”
-Daily scheduled medication
-Immediate effect
-Demand administration
B. Budesonide
C. Mommetasone
D. Fluticasone propionat
E. Cyclesonide
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-Most important class of “controllers”
-dysphonia, hoarseness
-Oropharyngeal candidosys
-pharyngitis
Systemic corticosteroids
Orally administered
-prednisone,prednisolone,metilprednisolone,etc.
-metilprednisoloneetc.
-Hydrocortisone hemisuccinate
Significant side effects: on long term therapy: metabolic (diabetes, proteic catabolism), digestive,
osteoporosis, immunodeficiency, HTA, cataract, suprarenal suppression, psychological, femoral necrosis,
obesity
Indications:
-Asthma exacerbations
Theophylline
-Modest antiinflamatory activity
-Bronchodilator effect
-Oral administration
Side effects: frequent nausea, vomiting, headache, tremor, digestive insomnia, psychological, tachicardia,
cardiac arrhytmia etc
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Long acting Beta 2 agonists (LABA)
Salmeterol
Formoterol
-Administration: Inhaled
-Inhibition ofbronchoconstriction
-Anti-eosinophillic effect
-Zafirlukast-2 tablets
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Clinical indication:
-Fenoterol
-Terbutaline,etc
Doses:
Oral Beta 2 agonists have similar side effects, like cardiovascular stimulation, tremon, hypokalemia,
irritability and restlessness, but they can be more significant than for other therapies
They are indicated for patients who cannot use inhaled therapy
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Conclusions:
-Pacient’sanxiety regarding inhaled medication is unfounded, when balanced against the effects of parenteral
corticotherapy
Systemic Corticoids-i.v.”reliever”
Mode of action –effects of systemic corticotherapy
-i.v.administration
-100 mg la 6 h –methylprednisolone
Anticholinergics-”reliever”
-Ipratropium bromid(20/40/ g/puf)
-Association withfenoterol
Conclusions:
Therapeutic strategy
Control of symptoms, not the cure of asthma
-Minimal symptoms (nocturnal)
-Minimize exacerbations
Step down
treatment visit at 3-6 months
if symptom cntrol is optained for more than 3 months a step down therapy may be proposed
Step up
if symptom control is not obtained
before everything else: verify if the medication is correctly administered by the patient, the patient‘s
compliance to treatment and check for potential enviromental triggers
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